Despite considerable accumulated information on pneumonia, the local inflammatory response to pulmonary infection is not understood. We know neither what happens at the initial site of infection in the first hours and days nor what determined the subsequent course in seemingly normal individuals. While properties of the organisms are surely important, it also seems likely that a proper variety and sequence of host protective reactions is critical. Such reactions might logically include; 1) exudation of complement, which if activated by either the classic or alternate pathway would act as a chemotactic substance for alveolar macrophages, blood monocytes, or polymorphonuclear leukocytes, 2) opsonization of bacteria by antibody or complement, 3) secretion of bactericidal antibody into the bronchopulmonary secretions, and 4) immigration and activation of alveolar macrophages. Our approach to these questions will be to study pneumonia in animals. Pneumonia will be produced in guinea pigs and rabbits by percutaneous puncture of the trachea and instillation of Streptococcus pneumoniae (type I or XXV), or Pseudomonas aeruginosa suspended in hog gastric mucin or Klebsiella pneumoniae in saline. Bronchopulmonary secretions will be assayed for chemotactic substances, opsonic activity (in the aqueous as well as surfactant fraction), the presence of complement, adherence of either complement or immunoglobulins to the surface of bacteria, and the presence of bactericidal antibody. Animals will be sacrificed serially so that differences in local responses with time may be determined. Furthermore, animals deficient in complement components and animals immunized by application of homologus killed organism to the respiratory tract will be studied to further elucidate the role of these factors.